Abstract
Liver histopathology of segmental portal ischemia occurring over a long-term period has not been previously described. For these reasons histological changes in the rat liver were studied from 1 h to up to 90 days after a left lateral and middle segmental portal obstruction. Within 3 h, the hepatocytes showed glycogen depletion in Rappaport zones 1 and 2 and pericentral and central lobular congestion of sinusoids and veins, whereas within 3 days, vein thrombosis appeared in the center of the lobule and liver necrosis was observed in Rappaport zones 2 or 3 or both, followed by restitutio ad integrum of the liver lobule morphology after 20-40 days. These results can be explained in light of two conditions occurring in the rat liver: (i) the peculiar low sensitivity of the liver to O2 debit and the protective or vasoactive effects used during hypoxia; and (ii) the sinusoidal network as a collateral source of the hepatic vascular system. Therefore, morphological assessment of this arteriolar and sinusoidal system, implicated in assuring efficient collateral blood supply in the rat liver with portal ischemia, is essential for understanding the mechanisms behind a natural and timely repair of ischemic injuries in the human liver.
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